title: Dynamic and dual effects of glycated hemoglobin on estimated glomerular filtration rate in type 2 diabetic outpatients.
abstract: BACKGROUND
  Diabetic nephropathy is the leading cause of incident end-stage renal disease in Taiwan. Previous studies on the consistent benefits of glycemic control in diabetic nephropathy focused primarily on delaying microalbuminuria. However, this effect on glomerular filtration rate (GFR) remains controversial. This study aims to establish a model that explains the controversial effects of glycated hemoglobin (HbA1C) on GFR.
  
  
  METHODS
  This retrospective cohort study followed subjects with type 2 diabetes mellitus, who were enrolled between June 2006 and December 2006, for 4 years. The effects of HbA1C on estimated GFR (eGFR) were examined both cross-sectionally and longitudinally. The dual effects of HbA1C on eGFR, and how renal function interferes with these effects, were investigated.
  
  
  RESULTS
  Of the 1,992 subjects enrolled, 1,699 completed the follow-up. HbA1C was positively correlated with eGFR in the cross-sectional study (β coefficient = 1.44, 95% CI: 0.71-2.17, p = 0.0001). In the longitudinal study, higher baseline HbA1C resulted in a greater decline in eGFR. The annual eGFR decline rates were -1.89, -1.29, and -0.68 ml/min/1.73 m(2)/year for baseline HbA1C >9, 7 to ≤9, and ≤7%, respectively. The eGFR value was simultaneously affected by concurrent (β coefficient = 0.78, 95% CI: 0.48-1.08, p < 0.0001) and preceding HbA1C (-0.52, -0.82 to -0.23, p < 0.0001). The positive effects of concurrent HbA1C on eGFR reached statistical significance at all stages of chronic kidney disease (CKD); however, the negative effects of preceding HbA1C only applied to CKD stages 3 and 4.
  
  
  CONCLUSIONS
  We developed a new model that demonstrates how preceding and concurrent HbA1C simultaneously affect eGFR in opposing ways. The dynamic effects varied among different CKD stages. The deterioration in eGFR at CKD stages 3 and 4 may be postponed by intensive glycemic control. Further prospective studies may be necessary to clarify the specific CKD stage(s) that will benefit from intensive glycemic control.
authors.affiliation: Divisions of Endocrinology and Metabolism, Department of Internal Medicine, Taichung Veterans General Hospital, Taichung, Taiwan, ROC.
authors.forename: Chia-Lin
authors.initials: CL
authors.lastname: Lee
authors.forename: Tsai-Chung
authors.initials: TC
authors.lastname: Li
authors.forename: Shih-Yi
authors.initials: SY
authors.lastname: Lin
authors.forename: Jun-Sing
authors.initials: JS
authors.lastname: Wang
authors.forename: I-Te
authors.initials: IT
authors.lastname: Lee
authors.forename: Li-Nien
authors.initials: LN
authors.lastname: Tseng
authors.forename: Yuh-Min
authors.initials: YM
authors.lastname: Song
authors.forename: Shang-Feng
authors.initials: SF
authors.lastname: Tsai
authors.forename: Wayne H-H
authors.initials: WH
authors.lastname: Sheu
mesh_terms: D000368:Aged; D015331:Cohort Studies; D003430:Cross-Sectional Studies; D003924:Diabetes Mellitus, Type 2 / Q000150:complications*; D003928:Diabetic Nephropathies / Q000097:blood / Q000209:etiology / Q000503:physiopathology*; D018450:Disease Progression; D005260:Female; D005919:Glomerular Filtration Rate; D006442:Glycated Hemoglobin; D006801:Humans; D008137:Longitudinal Studies; D008297:Male; D008875:Middle Aged; D051436:Renal Insufficiency, Chronic / Q000097:blood / Q000209:etiology / Q000503:physiopathology*; D012189:Retrospective Studies
chemical_list: D006442:Glycated Hemoglobin; C517652:hemoglobin A1c protein, human